The projects are designed to give information related to the: 1) intracellular mechanisms responsible for the rapid decline of cardiac contractility during ischemia and 2) factors determining the behavior of these mechanisms such as ontogenetic differentiation of striated muscle types. The effects of changes in intracellular ionic conditions and energy stores (H+), (MgATP 2 minus), known to be associated with ischemic negative inotropism will be determined on Ca2+-activated contractile protein force generation, Ca2+-cycling by the sarcoplasmic reticulum, and rate of Ca2+-activated force generation of skinned (sarcolemma disrupted or removed) muscle fibers. Comparative studies of skeletal and cardiac fibers will be done because of the known differential effect of ischemia on striated muscle types. The effects of acidosis and MgATP 2 minus depletion on skinned fiber Ca2+-activated force generation will be determined for cardiac, adductor magnus, and soleus fibers of 26-day embryo, 5-day newborn, and adult rabbits. Pieces of the same fibers will be characterized histochemically (myofibrillar ATPase, normal and ischemic twitch-tetanic force characteristics will be measured for each development phase. Data from these studies should also give information related to the mechanistic differences between the various skeletal muscle types.